A protein called tubulin (green) accumulates in the center of a nucleus (outlined in pink) from an aging cell. Normally, this protein is kept out of the nucleus with the help of gatekeepers known as nuclear pore complexes. But NIGMS-funded researchers found that wear and tear to long-lived components of the complexes eventually lowers the gatekeepers' guard. As a result, cytoplasmic proteins like tubulin gain entry to the nucleus while proteins normally confined to the nucleus seep out. The work suggests that finding ways to stop the leakage could slow the cellular aging process and possibly lead to new therapies for age-related diseases.
Featured in the February 18, 2009, issue of Biomedical Beat. Maximiliano D'Angelo and Martin Hetzer, Salk Institute